Myocardial energetics and diastolic dimensions of the heart in experimental hypertension.

The present study examined changes in left ventricular design and function in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY), and in SHR exposed to voluntary physical exercise in running wheels (R-SHR) and their respective sedentary controls (C-SHR). End-diastolic volumes were obtained in vitro by determining the pressure-volume relationships of isolated hearts arrested in diastole. Cardiac function and myocardial oxygen consumption were also assessed in vitro by means of an antegrade working heart perfusion technique. Compared with WKY and C-SHR respectively, ordinary SHR and R-SHR had increased end-diastolic volumes, whereas the ratios between wall thickness and internal radius were relatively unchanged. Maximal cardiac performance was elevated in the structurally enlarged SHR heart compared with WKY, whereas it remained unchanged after chronic physical exercise. Long-term voluntary running in SHR caused an elevation of cardiac output due to an increased stroke volume, while arterial pressure was unaltered. The stimulus for the cardiac redesign to a structurally enlarged heart can probably best be explained by a chronic elevation in cardiac filling. Hence, enlarged left ventricles can then produce higher stroke volumes for given degrees of myocardial fibre shortenings. Thus, despite structurally enlarged left ventricles in SHR and in R-SHR and also increased arterial pressure in SHR compared with WKY (thereby elevating systolic wall stress), cardiac function was maintained and even augmented, which was not associated with an increase in total myocardial oxygen consumption.